Evidence map›Paper›PMID 29531349›Full record

ArticleScientific reports2018

Insulin mediates de novo nuclear accumulation of the IGF-1/insulin Hybrid Receptor in corneal epithelial cells.

Rossella Titone, Meifang Zhu, Danielle M Robertson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  8. Teprotumumab improves light sensitivity in patients with thyroid eye disease.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024
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  18. IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Rossella TitoneThe Department of Ophthalmology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.ORCID 0000-0002-1528-331X
Meifang ZhuThe Department of Ophthalmology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Danielle M RobertsonThe Department of Ophthalmology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA. Danielle.Robertson@UTSouthwestern.edu.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

Effects of Systemic Disease on Corneal Epithelial PathophysiologyR01EY024546 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DANIELLE M. ROBERTSON · 2015 to 2026
$4.3M
Core Grant for Vision ResearchP30EY020799 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI NIEDERKORN, JERRY · 2010 to 2016
$4.1M
Interactive effects of OSA and T2DM on corneal and ocular surface diseaseR21EY024433 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI ROBERTSON, DANIELLE M. · 2014 to 2015
$433k
NEI NIH HHS P30 EY020799NEI NIH HHS R01 EY024546NEI NIH HHS R21 EY024433
6 · The paper itself

Abstract

Insulin and insulin-like growth factor-1 (IGF-1) are present in human tears and likely play an important role in mediating ocular surface homeostasis. We previously characterized the IGF-1/insulin hybrid receptor (Hybrid-R) in corneal epithelial cells and found that it was activated by IGF-1 and not insulin; and reported the novel finding that it localized to the corneal epithelial cell nucleus. Since the corneal epithelium is an insulin insensitive tissue and does not require insulin for glucose uptake, this study investigated the function of insulin in corneal epithelial cells. We show that stress induced by growth factor deprivation triggers transcriptional upregulation and de novo nuclear accumulation of Hybrid-R through the homodimeric insulin receptor (INSR). This occurs independent of PI3K/Akt signaling. Nuclear accumulation of Hybrid-R was associated with partial cell cycle arrest and a corresponding reduction in mitochondrial respiration. Treatment with insulin, and not IGF-1, attenuated IGF-1R and INSR transcription and restored cell cycle and metabolic homeostasis. Together, these findings support that insulin mediates receptor homeostasis in corneal epithelial cells, favoring an IGF-1 mediated pathway. This may have important implications in diabetic corneal disease and wound healing.

Indexed as

AnimalsCell Cycle CheckpointsCell NucleusEpithelial CellsEpithelium, CornealHomeostasisHumansInsulinReceptor, IGF Type 1Receptor, InsulinInsulinReceptor, IGF Type 1Receptor, Insulin

Identifiers

PMID29531349
PMCPMC5847585
OpenAlexW2806156470

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.